**Author details**

*Type 2 Diabetes - From Pathophysiology to Cyber Systems*

**4. Conclusions and future direction**

respectively.

lar level.

**Acknowledgements**

**Conflict of interest**

reported that food rich in saturated fat and triglyceride were found to have positive relationship on the increment of resistin concentration. Atherogenesis is a process of forming plaques in the intima layer of arteries. It developed progressively with inflammation and lipid accumulation varying significantly among individuals [75]. Thus, resistin provide macrophages with overly large lipid fractions inducing

As a summary, this chapter has explained on the relationship of food intake pathway and adipocytokine hormone effecting CVD in MetS. Adiponectin and resistin were found to have good correlation in the condition of high fat intake. High fat intake such as saturated fat and LDL food sources would potentially induce the level of resistin while polyunsaturated fatty acids and HDL food type potentially increase the level of adiponectin. High level of resistin and low level of adiponectin would contribute to the cardiovascular disease via AMPK and TLR4 pathways,

There were many studies done in investigating the action of adiponectine and resistin related to MetS and suggested various signaling pathways and mechanisms supporting effect of both protein hormones on CVD. Study believes that food intake would play a huge role in adjusting the level of adiponectin and resistin at various levels such as gene modification. Therefore, there is a scope for future studies to investigate narrowly on the mechanisms affecting adiponectin and resistin single nucleotide polymorphisms (SNPs) towards the development of Mets at cellu-

The authors would like to thank the Faculty of Medicine, Universiti Sultan Zainal Abidin (UniSZA) and Faculty of Health and Life Sciences, Management and

Science University (MSU) for providing the facilities and support.

The authors declare no conflict of interest.

dyslipidemia and result in the progress of atherosclerosis plaques.

**100**

Mimie Noratiqah Jumli1 and Muhammad Ilyas Nadeem<sup>2</sup> \*

1 Faculty of Medicine, Universiti Sultan Zainal Abidin (UniSZA), Kuala Terengganu, Terengganu, Malaysia

2 Faculty of Health and Life Sciences (FHLS), Management and Science University (MSU), Shah Alam, Selangor, Malaysia

\*Address all correspondence to: muhd\_ilyas@msu.edu.my

© 2021 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
